Responses of anterior hypothalamic-preoptic thermosensitive neurons to thyrotropin releasing hormone and cyclo(his-pro)

Hori, Tetsuro; Yamasaki, Mari; Asami, Toyoko; Koga, Hisao; Kiyohara, Toshikazu

doi:10.1016/0028-3908(88)90116-5

Cited by 30 publications

(16 citation statements)

References 24 publications

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“…In addition, a number of studies have shown that TRH injections into the POA, a well-recognized primary site for thermoregulation, cause hyperthermia in rats [46, 47]. It has been demonstrated that TRH inhibits heat-sensitive neurons and activates cold-sensitive neurons in the POA [48], a mechanism resulting in increased heat production and conservation. However, ablation of the POA did not block TRH antagonism of pentobarbital-induced hypothermia, suggesting that sites other than the POA may also mediate the thermogenic effect of TRH [49].…”

Section: Effects Of Trh On Bat Thermogenesismentioning

confidence: 99%

TRH Neurons and Thyroid Hormone Coordinate the Hypothalamic Response to Cold

Zhi¹,

Boelen²,

Kalsbeek³

et al. 2018

Eur Thyroid J

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Thyroid hormone (TH) plays a key role in regulating body temperature in mammals. Cold exposure stimulates the hypothalamus-pituitary-thyroid (HPT) axis at the hypothalamic level by activating hypophysiotropic thyrotropin-releasing hormone (TRH)-producing neurons, ultimately resulting in increased plasma TH concentrations. Importantly, the local TH metabolism within various cold-responsive organs enables tissue-specific action of TH on heat production and adaption to cold independently of the circulating TH levels. In addition to these neuroendocrine effects, TRH neurons in the hypothalamus also have neural connections with brown adipose tissue (BAT), probably contributing to regulation of thermogenesis by the autonomic nervous system. Recent studies have demonstrated that intrahypothalamic TH has profound metabolic effects on BAT, the liver, and the heart that are mediated via the autonomic nervous system. These effects originate in various hypothalamic nuclei, including the paraventricular nucleus (PVN), the ventromedial nucleus, and recently reported neurons in the anterior hypothalamic area, indicating a potential central function for TH on thermoregulation. Finally, although robust stimulation of the thermogenic program in BAT was shown upon TH administration in the ventromedial hypothalamus, the physiological relevance of these neurally mediated effects of TH is unclear at present. This review provides an overview of studies reporting the role of TH in cold defense, with a focus on recent literature evidencing the centrally mediated effects of TRH and TH.

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Section: Effects Of Trh On Bat Thermogenesismentioning

confidence: 99%

TRH Neurons and Thyroid Hormone Coordinate the Hypothalamic Response to Cold

Zhi¹,

Boelen²,

Kalsbeek³

et al. 2018

Eur Thyroid J

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“…The thyroid axis rapidly responds to cold stimulation by increasing thyroid hormone secretion in response to an increased release of TSH [8,9]. During cold exposure, TRH is enhanced in medial basal hypothalamus (MBH) push pull canula perfusates [10] as well as in peripheral blood [11], TRH has been postulated to be involved not only in the hormonal response to cold stress but also as a neuromodulator in the preoptic hypothalamic area, me-diating neural responses involved in thermogenesis [12,13].…”

Section: Introductionmentioning

confidence: 99%

Suckling and Cold Stress Rapidly and Transiently Increase TRH mRNA in the Paraventricular Nucleus

et al. 1993

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Thyrotropin releasing hormone (TRH) is released from the median eminence in response to neural stimuli evoked by different physiologic conditions (i.e. cold stress or suckling). The paraventricular nucleus (PVN) synthesizes pro-TRH and responds to negative thyroid hormone feedback. With the aim of determining if TRH biosynthesis is regulated in coordination with its release, we quantified TRH mRNA levels in PVN and in preoptic area-anterior hypothalamus (POA-AH) of rats sacrificed at different times during cold (0.5, 1,2 or 6 h) or suckling (15, 30 and 60 min) stimulus; TRH-like immunoreactivity (TRH-LI) in medial basal hypothalamus (MBH) and in POA-AH as well as corticosterone, triiodothyronine and prolactin levels in serum were also measured. Increases of serum hormones were observed in both paradigms as has been reported. MBH TRH-LI content decreased during suckling by 33% (p < 0.01) after 1 h, but did not change after cold stimulation. At short stimulation times, PVN TRH mRNA levels were 85% (30 min of suckling) and 97% (1 h in the cold) higher than their respective controls, decreasing to normal after 1-2 h. In the POA-AH, another TRH synthesizing region not involved in TRH hypophysiotropic function, a similar transient enhancement of TRH mRNA (146%) was observed only in cold stimulated animals after 30 min, consistent with its suggested role in thermogenesis. These results show a fast and transient response of TRH mRNA in PVN evoked by a neural stimulus.

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“…Indeed, TRH administration in the PVN increased body temperature in a rather prompt and sustained way. Although our estimated dose of TRH administration (0.2 μg/h) was rather low compared to other studies (0.1-40 μg single injection) [4,16,[26][27][28] , long-term exposure to TRH could result in downregulation of TRH receptors, which may account for the slight drop in temperature after 40 min of TRH infusion ( Fig. 4 b).…”

Section: Discussionmentioning

confidence: 47%

“…In experiments 2A and 2B, three blood samples were taken at -25, -20, and 0 min for basal glucose and corticosterone measurement. At time 0 (between 12: 00 and 13: 45), TRH (40 m M , Sigma-Aldrich, Germany) or Ringer's solution was perfused via the MD probes into the PVN at a speed of 3 μL/h for 2 h. The dose and route of TRH perfusion chosen in the present study will result in an estimated dose of 0.2 μg/h, which is within the lower range of other TRH studies in rat (0.1-40 μg single injection) [4,16,[26][27][28] , but comparable to the TRH concentration during cold exposure (35-45 pg/15 min) as measured by push-pull perfusion [22] . Blood samples of 100 μL were withdrawn every 20 min, and blood glucose concentrations were determined.…”

Section: Methodsmentioning

confidence: 76%

Administration of Thyrotropin-Releasing Hormone in the Hypothalamic Paraventricular Nucleus of Male Rats Mimics the Metabolic Cold Defense Response

et al. 2018

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Background: Cold exposure increases thyrotropin-releasing hormone (TRH) expression primarily in the hypothalamic paraventricular nucleus (PVN). The PVN is a well-known hypothalamic hub in the control of energy metabolism. TRH terminals and receptors are found on PVN neurons. We hypothesized that TRH release in the PVN plays an important role in the control of thermogenesis and energy mobilization during cold exposure. Methods: Male Wistar rats were exposed to a cold environment (4 ° C) or TRH retrodialysis in the PVN for 2 h. We compared the effects of cold exposure and TRH administration in the PVN on plasma glucose, corticosterone, and thyroid hormone concentrations, body temperature, locomotor activity, as well as metabolic gene expression in the liver and brown adipose tissue. Results: Cold exposure increased body temperature, locomotor activity, and plasma corticosterone concentrations, but blood glucose concentrations were similar to that of room temperature control animals. TRH administration in the PVN also promptly increased body temperature, locomotor activity and plasma corticosterone concentrations. However, TRH administration in the PVN markedly increased blood glucose concentrations and endogenous glucose production (EGP) compared to saline controls. Selective hepatic sympathetic or parasympathetic denervation reduced the TRH-induced increase in glucose concentrations and EGP. Gene expression data indicated increased gluconeogenesis in liver and lipolysis in brown adipose tissue, both after cold exposure and TRH administration. Conclusions: We conclude that TRH administration in the rat PVN largely mimics the metabolic and behavioral changes induced by cold exposure indicating a potential link between TRH release in the PVN and cold defense.

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Responses of anterior hypothalamic-preoptic thermosensitive neurons to thyrotropin releasing hormone and cyclo(his-pro)

Cited by 30 publications

References 24 publications

TRH Neurons and Thyroid Hormone Coordinate the Hypothalamic Response to Cold

TRH Neurons and Thyroid Hormone Coordinate the Hypothalamic Response to Cold

Suckling and Cold Stress Rapidly and Transiently Increase TRH mRNA in the Paraventricular Nucleus

Administration of Thyrotropin-Releasing Hormone in the Hypothalamic Paraventricular Nucleus of Male Rats Mimics the Metabolic Cold Defense Response

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